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    Chair of Microbiology

    Phagosomal Escape of Staphylococcus aureus

    Upon internalization by professional phagocytes (e.g. neutrophils ) and non-professional phagocytes such as endothelial or epithelial cells some Staphylococcus aureus strains are capable of escaping from the phagosome. This process has been hypothesized to contribute to chronic infection of the pathogen.

    Within this project we are investigating virulence factors involved in this evasive strategy of S. aureus.

    By means of a fluorescence microscopy approach we can determine the number of bacteria that escaped from the phagosome and reside in the host cell cytoplasm . Within the cytoplasm the bacteria divide and host cell death commences shortly thereafter By this approach we identified amphiphilic bacterial peptide toxins , phenol-soluble modulins – especially PSMα – which are required for efficient phagosomal escape (Grosz, et al. 2014).

    In a screen for other factors involved in escape we identified S. aureus mutants in the non- ribosomal peptide synthetase (NRPS) AusAB (also termed pznAB ). Mutants within this protein complex were less efficiently escaping from phagosomes thereby hinting at an involvedment of the dipeptide products of the underlying biosynthetic machinery (Blättner et al., 2016).

    Further we recently employed a screening procedure by which a highly complex Transposon mutant library pool was employed to screen for bacteria that were rendered unable to kill their respective host cells after internalization . In this research we identified the involvement of Rsp , an AraC -type transcriptional regulator in virulence of S. aureus. Interestingly , the Rsp-driven style='mso-spacerun:yes'>  transcriptome involves various virulence factors and Rsp is directly involved in transcription of a long non- coding RNA (Das et al. 2016).

    Intracellular Staphylococcus aureus (red) is labeled by the escape marker (green) when it translocates to the host cell cytoplasm.
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